86
PLUTONIUM
3. HEALTH EFFECTS
1998). Suslova et al. (2006) measured urinary plutonium excretion
and terminal body burdens in
187 healthy plutonium workers. When expressed as a fraction of terminal body burden (measured at
autopsy), the mean excretion rate was 1.5x10
-5
d
-1
(GSD=1.78); this corresponds to a urinary elimination
half-time of approximately 127 years. The excretion rates were higher in workers who died of
malignancies, cardiovascular or respiratory tract disease (2.1x10
-5
d
-1
, half-time: 90 years), or liver
disease (2.6x10
-5
d
-1
, half-time: 73 years). Excretion rates among workers exposed primarily to more
soluble forms of plutonium (e.g.,
plutonium nitrate; 1.4x10
-5
d
-1
, half-time: 136 years) were
approximately twice those of workers exposed primarily to plutonium metal and oxides (0.7x10
-5
d
-1
,
half-time: 271 years). Kathren and McInroy (1991) analyzed data on urinary excretion of plutonium and
postmortem tissue levels in five plutonium workers (four of whom were exposed to plutonium by the
inhalation route) and concluded that body burdens were consistent with biphasic urinary elimination
kinetics with approximate half-times of 40 and 100 years. Etherington et al. (2003) measured urinary and
blood plutonium kinetics in two adult subjects who inhaled an aerosol of
237+244
Pu(NO
3
)
4
(AMAD=1.1 μm; GSD=1.2). Urinary clearance (expressed as a fraction of blood plutonium burden
excreted per day) ranged from 0.03 to 0.1 d
-1
during the first 30 days following exposure (corresponding
half-times are 7–23 days). Medical follow-up studies have been conducted on
persons exposed to
plutonium during work related to the Manhattan Project (Voelz and Lawrence 1991; Voelz et al. 1979,
1985, 1997). Leggett (1985) reported an analysis of a subset of 12 subjects (Voelz et al. 1979), 30 years
following the conclusion of the exposure period, and estimated urinary and fecal clearance (fraction of
blood burden) to be 0.06 and 0.024 d
-1
, respectively (corresponding half-times are approximately 12 and
29 days).
Studies conducted with nonhuman primates have confirmed that the relatively slow excretion and
elimination kinetics of inhaled plutonium arise from long retention times in lung, liver, and skeleton
(Brooks et al. 1992; LaBauve et al. 1980; Lataillade et al. 1995; Metivier et al. 1978b; Stanley et al.
1982). Studies conducted in dogs (i.e., beagles) have shown that lung retention is a greater contributor to
slow elimination of
239
PuO
2
than it is for
238
PuO
2
,
238
Pu(NO
3
)
4
, or
239
Pu(NO
3
)
4
, which are
more rapidly
absorbed and distributed to the liver and skeleton. In beagles, during the first few days following
inhalation exposure to PuO
2
or Pu(NO
3
)
4
, fecal excretion is the dominant excretory pathway, reflecting
mucociliary clearance of deposited plutonium to the gastrointestinal tract where the absorbed fraction is
relatively low (e.g., <1%). Following this period of relatively rapid clearance of plutonium from the
respiratory tract, fecal excretion declines and urinary excretion makes a larger contribution to elimination
of the body burden, equaling or exceeding fecal excretion (Bair et al. 1973; Mewhinney and Diel 1983).
However, both fecal and urinary excretion rates (percent of body burden/day) decline over time and vary
87
PLUTONIUM
3. HEALTH EFFECTS
with different chemical and physical forms and isotopes of plutonium. Bair et al. (1973) compared
urinary excretion kinetics during the first 100 days following exposures of beagles to
239
PuO
2
(MMD 1–
5 μm),
239
PuO
2
(MMD 0.1 μm),
238
PuO
2
(MMD 0.1 μm), or
239
Pu(NO
3
)
4
(MMD 0.12 μm).
Urinary
excretion of plutonium (per cent of body burden, 50–100 days postexposure) following exposure to
239
PuO
2
(MMD 1–5 μm) was slower (≈5–10x10
-5
% body burden/day) than following exposure to
239
PuO
2
(MMD 0.1 μm; ≈1x10
-3
% body burden/day),
238
PuO
2
(≈2–3x10
-3
% body burden/day) or
239
Pu(NO
3
)
4
(≈1–
2x10
-2
% body burden/day).
3.4.4.2 Oral Exposure
Enhanced urinary excretion of
239+240
Pu was observed in humans during 7
days following ingestion of
mollusks containing
239+240
Pu (Hunt 1998; Hunt et al. 1986, 1990). Excretion of plutonium in urine was
also observed in the first 24 hours following an oral dose of
236
Pu(VI) bicarbonate (or
239
Pu(VI)
bicarbonate) administered to baboons (USNRC 1992). Priest et al. (1999) observed urinary excretion of
plutonium in a human who ingested plutonium-contaminated sediments. Studies conducted in
dogs and
various rodent species have shown that following ingestion, absorbed plutonium is excreted in urine
(Sullivan 1980a; Sullivan et al. 1985).
3.4.4.3 Dermal Exposure
Occupational accidents have resulted in dermal exposures and/or penetration
of plutonium into skin
wounds and subsequent systemic absorption of plutonium (McInroy et al. 1989; Woodhouse and Shaw
1998). In one case, postmortem measurements of
239
Pu levels in tissues, measured 17 years following the
incident, showed that liver contained approximately 41% of the body burden and skeleton contained 49%
of the body burden (McInroy et al. 1989). Woodhouse and Shaw (1998) reported urinary excretion of
plutonium during 20–30-year periods following various wound-related
exposures to PuO
2
(oxalate),
Pu(NO
3
)
4
, or plutonium metal. Slow-phase urinary excretion half-times for six subjects ranged from 17 to
34 years.
3.4.4.4 Other Routes of Exposure
Plutonium excretion and tissue distributions (postmortem) have been measured following intravenous
injection of Pu(IV) citrate (Langham et al. 1980; Talbot et al. 1997). Various analyses and summaries of
the data from Langham et al. (1980) have been published (AEC 1971; Durbin 1972; Kathren 2004;
Leggett 1985). Postmortem tissue plutonium measurements for seven subjects have been reported; data